7-9% proteins 90% water 0. 1% sugar 0. 03% urea 0. 9% salt

reduction of Hb in blood (not necessarily red cells) red cell reduction is indicative of marrow failure anaemic pt have below average Hb

Normal Hb production Genetic mutation of globin chains α chains (Asian) β chains (Mediterranean) Clinical features include Chronic Anaemia Marrow Hyperplasia Spenomegaly Cirrhosis Gallstones Treated w/ blood transfusions Prevent iron overload

Haematology p186 Flashcards by niamh ritchie

components of blood

plasma 55%

red blood cells 44%

WBCs, platelets 1%

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plasma components

7-9% proteins

90% water

1% sugar
03% urea
9% salt

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red blood cells

carry oxygen and Hb

release ATP which cause vessel walls to relax to promote blood flow

when lysed pathogenically by bacteria the Hb in the RBC produces free radicals which break down the bacterial cell membrane destroying it

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anaemia is

reduction of Hb in blood (not necessarily red cells)

red cell reduction is indicative of marrow failure

anaemic pt have below average Hb

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av male Hb

13.5-17.5g/dl

anaemia male - <13g/dl

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av female Hb

12.0-15.5d/dl

anamic female 11.5g/dl

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general clinical features of anamia

hypoxia - compensatory changes = inc HR + SV = CO

pallor - due to vascular constriction in skin

fatigue

tachycardia (to try and make up for poor oxygen transport)

may develop a murmur

in elderly it can manifest as palpitations, dyspnoea, angina and signs of caridac failure

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histological classifications of anaemia

hypochromic microcytic (pale small cells)

iron def, thalassaemia, some chronic disease

normochromic normocytic (normal colour, normal size)

chronic disease (heart failure, renal failure), acute blood loss

macrocytic (large cells)

megaloblastic (B12, folate), aplastic, liver disease

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classes of anaemia

haematinic deficiency anaemias

haemaglobinopathy anaemias (globin chains)

marrow failure anaemias (reduced RBC)

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3 marrow failure anaemias

aplastic anaemia

acute leukaemia (neoplastic proliferation of leukocytes, usually disseminated)

lymphoma (neoplastic proliferation of leuokcytes, usually solid tumour)

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2 haemoglobinopathy anaemias

thalassaemia

sickle cell anaemia

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haematinic deficiency anaemia (2)

iron deficiency anaemia

perncious (B12) megaloblastic (B9/folate) anaemias (def B12 and folic acid)

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iron def anaemia

Causes include chronic blood loss, malabsorption of iron (coeliac disease), dietary deficiency, increased physiological demand (e.g pregnancy, puberty), Low ferritin (stores and releases iron)

Clinical features include

Kolinychia (concave nails)
Pruritus (itching)
Angular Stomatitis
Painless glossitis (beefy tongue)

Low Hb, Low MCV + MCH

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pernicious megaloblastic anaemias

def B12 and folic acid

Both B12 and Folic acid needed for DNA synthesis in maturing erythroblasts

Def. in either causes erythroblasts to have large nuclei= megaloblasts in marrow

B12 absorbed by intrinsic factor in terminal ileum

Folate absorbed in the duodenum

Clinical features include

Painful glossitis
Demyelination of the spinal cord
Peripheral neuropathy
Ataxia

Low Hb, High MCV

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Thalassaemia

Normal Hb production

Genetic mutation of globin chains

α chains (Asian)
β chains (Mediterranean)

Clinical features include

Chronic Anaemia
Marrow Hyperplasia
Spenomegaly
Cirrhosis
Gallstones

Treated w/ blood transfusions
Prevent iron overload

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sickle cell anaemia

β chain substitution

Changes shape in hypoxic environment (prevents passage of cells through capillaries)

Heterozygous- Sickle cell TRAIT
Homozygous- Sickle Cell DISEASE

Clinical features include

Vascular Occlusion
Retinal Ischaemia
Acute chest syndrome

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aplastic anaemia

Diminished or absent Haematopoetic precursors in bone marrow

Present as, Pancytopenia, Macrocytosis (inc. MCV), reticulocytopenia (immature RBCs)

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acute leukaemia

Accumulation of malignant white cells in bone marrow and blood

Malignant cells tend to be precursors (blast cells)

Two types Acute MYELOID leukamia and Acute LYMPHOBLASTIC leuakaemia

Neutropenic- ROU

Thrombocytopenia- Mucosal Bruising, Petechiae, epistaxis (nosebleed) and Gingival Hypertrophy

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lymphoma

Malignant lymphocytes accumulating in Lymph nodes

Lymphadenopathy, Peripheral vasculature, even organs

Nodular Lymphocyte-predominant Hodgkin’s Lymphoma (NLPHL) - malignant B cells lying in a meshwork of folicular dendritic cells and reactive lymphocytes

Classical Hodgkin’s Lymphoma- neoplastic B cells amongst Reed-Sternberg (RS) cells and plasma cells + eosinophils

Presence of RS cells determines whether it is a Hodgkin’s or Non-Hodgkin’s Lymphoma

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normal RCC

male

4.7-6.1 million cells/mcL

usually normal in anaemia

check if normochromic/cytic

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normal RCC

females

4.2-5.4 million cells/mcL

usually normal in anaemia

check if normochromic/cytic

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WCC normal

between 4.5 and 10.0 thousand cells/mcL

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MCV is

mean corpuscular volume (volume RBC’s take up, a.k.a size)

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normal MCV

87 +/- 5 femtolitres (fL)

will be normal in bleeding but reduced volume overall

HCT is

haematocrite % vol of RBC in blood

HCT in newborns

60% 0.6 varies in children

HCT in males

40-52% 0.4-0.52

HCT in females

46% 0.46 can be reduced in pregnancy

PLT is

platelets

normal PLT

150-400 thousand per mcL

ferritin in males

18-270mcg/L

ferritin in females

18-160mcg/L

polycythaemia

raised Hb

leukocytosis

raised WCC

thrombocythaemia

raised PLT

reasons for needing a blood transfusions

When one or more components of the blood has to be replaced quickly, i.e in blood loss * e.g RBCs, PLTs, Clotting factors When bone marrow can’t produce blood cells * e.g RBCs, PLTs

if have only just one odd number in bloods if multiple

reactive change? more likely pre neoplastic - investigate

how to blood transfuse

Sample taken from patient * ABO compatability * Rhesus +ve or -ve * Sometimes there are unknown antigens present Tested v donated sample, if matched = given to patient If poor match- fever, jaundice, fluid overload Prion Disease- neurogenerative conditions Bacteria (Syphilis) and Viruses (Hep B, C, HIV and TT viruses) can all be transmitted via transfusion of blood

porphirins are

proteins involved in Hb metabolism

2 main types of porphyria

hepatic porphyria erythropoetic porphyria

acute episodes of porphyria cause

purple urine, abdominal pain, seizures, skin rash from sunlight and psychosis

clotting factor VII def is

haemophilia A X chromosome recessive inherited bleeding disorder (higher male incidence)

clotting factor IX deficiency is

haemophillia B (christmas disease) mutaration of FIX gene on the X chromosome results in low/absent level of FIX gene in plasma

severtity of haemophilia A correlates to

level of Factor VIII in blood

DDAVP is

desmopressin can be usde to tx mild haemophilia and vWD by stimulating release of vWF

Von Williebrand's disease

vWD decrease in von Williebrand's factor which causes a reduced factor VIII level vWF acts as a carrier molecule for Factor VIII hence why it can't be degraded to be used in coagulation as it isn't near the site of insult reduced platelet aggregation

3 acquired bleeding disorders

disseminated intravascular coagulation DIC vit K deficiency hepatopathology

disseminated intravascular coagulation

Consumption of clotting factors widespread Causes microthrombi to form excess consumption of factors and platelets means intial coagulopathy then excess bleeding

vit k def due to

malabsorption in GIT

hepatopathology causes

reduced level of clottisng factors produced so bleeding disorder

acquired platelet disorders

Thrombocytopaenic disorders * Acute Idiopathic Purpura (Children) * following a viral infection * autoantibodies bind to platelets and cause them to be removed from circulation and destroyed by spleen * Myeloproliferative disorders * Bone marrow doesn’t produce enough platelets causing systemic low platelet count Acquired disorders of platelet function * Antiplatelet agents

antiplatlet agents

Aspirin inhibits Cyclo-oxygenase enzyme which is needed to synthesise thromboxane a2 which is needed to activate platelets Heparin Penicillins

hypercoagulation called

thrombophilia

heriditary thrombophilia

factor V Leiden mutation protein C protein S anti-thrombin III def

acquired thrombophilia

antiphospholipid syndrome (Hughs syndrome) caused by presence of Lupus anti-coagulant in blood sugery, trauma, immobilisation, cancer etc

increased platelets called

thrombocythaemia

essential throbocytosis

inc platelets v uncommon managed with aspirin

INR is

internal normalised ratio prothrombin time Ratio of patients clotting value over the normal clotting value Normal INR- = 1.0 Warfarin INR- 2.0-3.0 - people who have AF or leg/lung clots have higher INR ratio LOWER THE INR THE FASTER THE CLOTTING TIME